Blood flowing from the nostrils of competitive Thoroughbred horses has been observed as far back as the sixteenth century. And despite over three hundred years of recognition, the condition has remained an enigma and until recently little has been attempted or achieved to uncover the underlying etiology and pathogenesis of this condition.
Historically, the source of blood at the nostrils was assumed to originate from within the nasal cavity because of the highly vascular nature of this organ. Post-exercise horses who exhibit blood at the nostrils are designated as "bleeders" and the condition termed "epistaxis", mistakenly analogous to epistaxis in man. However, two concepts emerged from observations of this condition, namely, that the blood originated in the nasal cavity, and that a positive relationship existed between bleeding episodes and poor competitive performance.
A recent retrospective survey of post-exercising horses with clinical evidence of blood at the nostrils positively identified the source of blood to have originated from the lungs. And repeated occurrences of pulmonary hemorrhage were precipitated by competitive exercise only. Further support of the hypothesis of the lung being the source of the blood was determined in horses with indwelling tracheostomy tubes that bled while being raced, the blood exiting the respiratory tract via the tracheostomy. By temporarily closing the tracheostomy, the blood flowed from the nostrils.
In the past, the paucity of diagnostic instrumentation which would allow safe examination of the equine upper respiratory tract with minimal restraint has been the primary factor impeding elucidation of this equine problem. The recent availability of the flexible fibreoptic endoscope into veterinary medicine has not only facilitated examination of the equine respiratory tract but has provided a means of locating the source of blood in bleeding horses.
The appearance of blood at the nostrils in exercising horses ranges from less than 1 to as high as 12 percent, but is generally about 0.5 to 2.5 percent. However, endoscopic surveys worldwide indicate that the actual prevalence of pulmonary hemorrhage is significantly higher than previously thought, with a range of 45 to 86 percent of racing or near maximal exercising horses. The incidence of pulmonary hemorrhage increases in direct proportion to the length of, and number of times, the endoscope is used on the individual animal. Histological examination of the caudal portion of the lung lobes revealed that 96 percent of horses that have raced had evidence of old alveolar hemorrhage.
The term used to describe the condition of pulmonary hemorrhage in horses without blood at the nostrils is exercise induced pulmonary hemorrhage (EIPH). EIPH is a more accurate description of bleeding in the racing horse than "bleeder". Multiple endoscopic surveys indicate that although pulmonary hemorrhage is experienced by a large number of racing or maximally exercising horses, epistaxis is a relatively infrequent manifestation of this phenomena. The frequency of occurrence of EIPH shows no relationship between the horse's sex, finishing position in the race, increasing age or distance raced. However, increased speed of exercise is directly associated with, and the common factor in, a higher incidence of EIPH in racing or maximally exercising horses.
Speeds greater than 240 meters per minute are necessary for a horse to have EIPH. The minimum speed required for a Standardbred to officially qualify to race competitively is about 755 meters per minute with the current world record about 885 meters per minute, whereas the average speed of racing Thoroughbreds is about 1050 meters per minute. EIPH occurs equally in both exercising Standardbreds and Thoroughbreds. However, the incidence of EIPH with epistaxis occurs only rarely in the racing Standardbred but more frequently in the racing Thoroughbred. Thus the speed of competition appears to be the constant factor designating whether a racing or maximally exercising horse will or will not have EIPH with epistaxis.
Repeated endoscopic examination of the same individual horse indicates that EIPH is not a random event but will repeatedly recur in the individual horse on a consistent basis. If a horse bleeds today, the chance of that same horse bleeding the next time it exercises or races is ten times higher than the horse who is not a bleeder. Periods of rest do not stop EIPH in horses. Upon return to training, and when maximal exercise form has been attained, bleeding recurs. Therefore, repeatability of EIPH is a consistent feature of this pathological phenomenon.
To determine the incidence of EIPH in post-racing horses, the animal was examined within 90 minutes of the completion of racing using a flexible fibreoptic endoscope. Both nostrils were examined for signs of hemorrhage. Other than the endoscopic observation of blood in the airways, a clear definitive set of clinical signs on which to establish a diagnosis of EIPH has not been documented. Astute horsemen report that horses with EIPH often have a distressed or anxious expression, "coolout" slowly, cough occasionally and swallow frequently. Coughing is not a consistent sign. Swallowing is a more consistent sign and is often the first indication of EIPH post-race. As the mucociliary blanket of the trachea clears the blood carried from the original source in the lungs, the blood pools on the floor of the larynx, flows onto the epiglottis, and then initiates the swallowing reflex.
Dyspnea is not commonly seen and if it occurs is a serious sign associated with extensive hemorrhage into the airways, exacerbation of pre-existing pulmonary disease or structural lung damage, ie. pulmonary abscess, pleural separation or tearing.
A characteristic pattern of clinical signs attributable to EIPH is further complicated by the variable response of the individual horse to the presence of blood in the airways. Moreover, the presence of blood at the nostrils is not a direct reflection of the severity of pulmonary hemorrhage or a determinant of the extent of the variability of performance noticeable upon initiation of pulmonary hemorrhage.
The major lesions of EIPH are multiple, separate and coalescing foci of moderately proliferative small airway disease accompanied by intense neo-vascularization of the bronchial circulation. These lesions are bilaterally symmetrical and confined to the dorsal angle of the lungs. Lesion extension occurs only along the dorsum of the lungs. Microscopic examination of the lungs of horses dying of EIPH has revealed engorgement of the pulmonary arteries, veins and capillaries, and rupture of the capillaries with hemorrhage into alveoli, bronchioles, bronchi, interstitium and subpleural tissue. The severity of engorgement and hemorrhage varied from almost nonexistent to massive in various areas of the lung, but the caudal portion of the lung lobes was the site of the most severe hemorrhage. Focally extensive pleural and interstitium fibrosis, and bronchiolitis were often accompanied by severe hemorrhage around large vessels and airways. Hemosiderophages also were present within this fibrous tissue, particularly at the junction of the pulmonary parenchyma and the deep layers of the pleura.
Latterly, numerous procedures have been performed in an attempt to prevent EIPH, with or without epistaxis, such as change of feed, bedding or ventilation, application of external or cold compresses to the nasal turbinate area, intermittent application of cold water over the thorax, and tying up the tail. More recently, various parenteral agents have been utilized in an effort to diminish the magnitude of EIPH in racing or near maximally exercising horses, namely atropine, estrogens, coagulants, clenbuterol (Ventipulmin.TM.), ipratropium (Atrovent.TM.), cromolyn (Intal.TM.), intravenous saline infusion and steam inhalation. Hesperidin-citrus bioflavinoids administered orally do not alter the prevalence of the pulmonary hemorrhage. Enforced rest, with a convalescence length much longer than three months duration, does not change the repeatability of the EIPH episodes which recur, with or without epistaxis, upon resumption of training and upon attaining maximal exercise form. But most of these techniques and treatments are no rarely utilized.
Currently, the sulfamoyl-anthranilic acid derivatives, for example, furosemide (Lasix.TM.) and ethacrynic acid, are parenterally administered to horses prior to racing in an attempt to control EIPH. Both of these drugs are potent diuretics which cause marked circulatory volume contraction in horses. The efficacy of these drugs in preventing EIPH has been extensively evaluated with widely variable results--sometimes stopping the hemorrhage, other times not stopping the hemorrhage, and yet at other times reducing the severity of the hemorrhage but not stopping the hemorrhage. Administration of these diuretics to horses having EIPH did not influence either the racing time or the systemic circulation physiology. However, administration of furosemide to horses negative for EIPH enhanced racing performance.
All the aforementioned procedures and drugs have been used in an attempt to prevent EIPH in exercising horses without fully understanding the underlying pathophysiology. EIPH, with or without epistaxis, in racing or maximally exercising Thoroughbred or Standardbred horses, causes greater financial losses than is encountered in other breeds of horses. Monetary loss following an EIPH episode ranges from slight to severe. EIPH occasionally can be fatal with affected horses dying almost instantaneously, this fatality often occurring during the latter portion of a race. But all affected EIPH horses are sub]ect to an economic loss of some degree. In spite of a multiplicity of endeavours used to minimize EIPH in racing or maximally exercising horses, it remains today a major worldwide problem in the horse racing industry.
Commercially formulated horse diets for strenuously exercising animals contain only naturally occurring feed ingredients and thus have high protein and energy levels. The protein level is adequate without the addition of non-protein nitrogen (NPN) in any form. Usually, at time of manufacture, or immediately prior to feeding, the animal's diet may be supplemented with vitamins and minerals. Regardless of the time of supplementation, only small amounts of alkaline potassium salts, if at all, may be added to the manufactured feed. Potassium, in large concentration, is normally present in all forages, grains and grain by-products. The availability of potassium to simple stomached animals is about 85 to 90 percent. Thus an animal's recommended daily potassium requirement is readily acquired through the daily feed intake and potassium deficiency symptoms infrequently develop. Consequently, potassium supplementation of the horse's daily feed is neither routinely implemented nor required.
The following reference discloses subject matter which is relevant to exercise-induced pulmonary hemorrhage: M. W. O'Callaghan et al., "Exercise-Induced Pulmonary Hemorrhage in the Horse: Results of a Detailed Clinical, Post-Mortem and Imaging Study", Equine Veterinary Journal (1987) 19(5), 384-434.